Dysbarisms and Other Selected Health Effects

Common Dysbarisms

Divers face an array of unique health hazards. The first two effects below are associated with hyperbaric conditions; the latter three occur due to changing pressures:

Gas narcosis caused by nitrogen in normal air dissolving into nervous tissue during dives of more than 120 feet [35 m]. Helium, substituted for nitrogen in "mixed-gas diving," can cause an effect called High Pressure Nervous Syndrome beyond 500 feet of salt water (fsw). [more...]

Gas toxicities caused by oxygen and carbon dioxide. The damage of oxygen to the lung and brain will vary with partial pressure above one atmosphere and time of exposure and is a concern when the molar fraction of oxygen is increased, as in NITROX diving. The effect of carbon dioxide changes from a respiration stimulant at normal partial pressures of 15-40 mm Hg to a respiration suppressor above 80 mm Hg. [more...]

Pain due to expanding or contracting trapped gases, potentially leading to Barotrauma. This acute symptom and potential damage can occur either during ascent or descent, but are potentially most severe when gases are expanding.

Decompression sickness [DCS] due to the evolution of inert gas bubbles, in vivo. Acute symptoms of DCS can occur during a decrease in pressure, but they occur most commonly soon after the ascent has been completed.

Dysbaric Osteonecrosis is detectable bone lesions most commonly on the body's long bones. Although its etiology is unknown, this chronic disease may be related to the evolution of gas bubbles that may or may not be diagnosed as a decompression sickness.

Most dysbarisms are predictable using some combination of Boyle's Law, Dalton's Law, and/or Henry's Law. Boyle's Law applies to the expansion and contraction of gases within the body because of external pressure changes due to depth. Dalton's Law states that in a mixture of n gases the partial pressure of each gas [Pi] is proportional to the molar fraction of each gas [Yi] that makes up the total, and can be used to determine how much nitrogen, oxygen, or carbon dioxide is in the ambient air at any hyperbaric pressure underwater. Henry's Law states a gas will dissolve into a liquid in proportion to its partial pressure in the air and its solubility in the liquid, and can predict the body's absorption of inert gases into and back from the body at any pressure or depth.

Pain and barotrauma from expanding or contracting gases while transiting between pressure zones are the most direct effects predictable from Boyle's Law. The most common sites of pain from trapped gases are the digestive tract, sinuses, teeth, middle ear, and lungs (the latter particularly during ascent).(1, 3, 7, 16) Good dental care should avoid trapped gas in teeth. Divers and flyers should anticipate these effects and not attempt to suppress the release of natural digestive gases that will expand during ascent. Blockage of sinus passages due to nasal congestion or a head cold can cause pain during either ascent or descent. Sinus pain during descent is called "sinus squeeze." Divers should be trained to detect blocked sinuses and not dive with a cold or an allergic inflammation. The most common source of pain on descent is from the contraction of air in the middle ear if the eustachian tubes are inflamed or blocked. Divers should be trained to clear their ears every two feet, and to stop and rise back up a few feet before attempting to clear a blockage.(1, 13) The most severe outcome of expanding gases is pulmonary barotrauma. An increase in gas volume of 20 to 30 percent can cause an initially full lung to rupture. It is important to realize that the proportionate change in pressure and trapped gas volume (predictable by Boyle's Law) occurs over smaller distances at shallow depths than when starting from deeper depths.

Decompression sickness (DCS) is the most commonly known of the many dysbarisms. It is sometimes referred to as "evolved gas dysbarism," "compressed air sickness," "caisson worker's syndrome," or various common names listed in Table 2. DCS is completely different from the preceding direct effects. DCS is caused indirectly by the formation of inert gas bubbles (nitrogen or helium if used) at one or more locations within the body, corresponding to the symptoms. The gas is absorbed slowly at depth from the blood to the tissues. The amount of gas absorbed depends upon depth and "bottom time."(1, 3) During ascent, divers can easily decompress to lower pressures at rates much faster than the stored gases can be reabsorbed back into the blood and exhaled out of the body. If the pressure ratio is too large, bubbles form and symptoms of DCS occur, ranging from mildly irritating to severe. A simple medical classification of DCS has evolved. Type I DCS consists of only skin, lymphatic, or joint pain. DCS Type II involves respiratory symptoms, neurologic or auditory-vestibular symptoms, and shock or barotrauma symptoms. Type II DCS is potentially life-threatening. The incidence of DCS is largely unknown.(13, 17, 18)

Dysbaric Osteonecrosis (sometimes also called Aseptic Bone Necrosis) manifests itself as regions of bone and marrow necrosis, especially of the humerus, femur, or tibia.(13, 17, 19) The condition is generally asymptomatic, with detection relying on differential diagnosis of high-quality radiographs and by excluding other causes.(15, 18, 20) The prevalence of detectable bone lesions was reported as 6.2 percent among British divers.(17) Most lesions were in parts of the bone unlikely to cause symptoms; however, lesions at joints were found in 1.2 percent of divers. There are strong positive associations between lesions and length of diving experience (but not age), the maximum depth dived (in fact, none were found in those who had never dived below 30 m [100 feet]), and a history of at least one prior DCS (although it can also occur without any known prior acute DCS symptoms).(17) There is a tendency to assume that bone necrosis is caused by evolved gas bubbles that did not necessarily cause acute symptoms, but there is no direct evidence for any clear etiology. It is probably important to understand that existing decompression schedules have been defined and refined experimentally based on symptoms, rather than on preventing bubbles per se or by maintaining and applying good epidemiological health surveillance.(7)

Administratively limiting depth has been the most common control for nitrogen narcosis. Reducing nitrogen as the source by using enriched oxygen mixtures (called NITROX) can be a cost-effective control by speeding the ascent rate, thus decreasing the total diving time. However, it is limited to a shallower depth than air diving because of oxygen's own toxicity at pressures of more than one atmosphere.(3)

Substituting helium for all or most of the nitrogen (called "mixed gas diving") is a cost-effective control for surface supplied He/O2 dives down to 380 feet of salt water (fsw). Dives beyond that are only practical by keeping the diver under pressure for several days (called "saturation diving"). The rate of compression must be kept slow to avoid symptoms of High Pressure Nervous Syndrome, such as nausea, fine tremors, and incoordination that can begin to appear at about 500 fsw.(1, 2, 13) Dives deeper than 1000 fsw have been made using a tri-mix of nitrogen, helium, and oxygen.(2)

The risk of DCS is controlled by administratively limiting the pressure ratio during ascent through the use of decompression schedules, such as those published in the US Navy Diving Manual(1, 2) or the NOAA Diving Manual.(3) These manuals also define short dives that may be made with no decompression time. The substitution of helium for nitrogen changes the rates of gas exchange and the decompression schedule, but does not remove the bubble hazard. Motivational training and close supervision of decompression schedules are essential components of a successful diving program. The use of one atmosphere suits is a recent development that has some promise if issues of functional flexibility can be overcome.(15)

Oxygen and Carbon Dioxide toxicity

Most symptoms of oxygen toxicity can be categorized into either pulmonary (coughing, substernal soreness, and pulmonary edema) or central nervous system (including body soreness, nausea, muscular twitching, and convulsions).(4, 5, 7, 14) Oxygen toxicity effects to the central nervous system are more common in the time-frame of a working day, while pulmonary effects are more of a concern during saturation diving.(7) The preferred control is to maintain the oxygen partial pressure close to 0.21 absolute pressure at sea level (ATA), and administratively limiting the time of exposure above one atmosphere.(2, 13)

Carbon dioxide becomes toxic when it suppresses respiration. Normally an increase in PCO2 decreases blood pH, which acts to increase the respiratory rate. However, at PCO2 >80 mm Hg (about twice the IDLH), the respiratory control center becomes depressed and will soon cease to function.(15) Such partial pressures only occur from the accumulation of exhaled carbon dioxide at increased pressure (either in the breathing system's dead space or due to a system malfunction). OSHA regulations for commercial diving (1910.430 and 1926.1090) limit CO2 to 1000 ppm in supply air and to "0.02 ATA" within the mask, usually by assuring that the flow of surface supplied air to masks and helmets is at least 4.5 actual cubic feet per minute (acfm) at any depth.

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